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Inhibition of phosphatidylinositol 3-kinase and protein kinase C attenuates extracellular matrix protein-induced vascular smooth muscle cell chemotaxis 

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Presentation on theme: "Inhibition of phosphatidylinositol 3-kinase and protein kinase C attenuates extracellular matrix protein-induced vascular smooth muscle cell chemotaxis "— Presentation transcript:

1 Inhibition of phosphatidylinositol 3-kinase and protein kinase C attenuates extracellular matrix protein-induced vascular smooth muscle cell chemotaxis  Alliric I. Willis, MD, Shoichi Fuse, MD, Xiu Jie Wang, MD, Emery Chen, BA, George P. Tuszynski, PhD, Bauer E. Sumpio, MD, PhD, Vivian Gahtan, MD  Journal of Vascular Surgery  Volume 31, Issue 6, Pages (June 2000) DOI: /mva Copyright © 2000 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

2 Fig. 1 Chemotaxis concentration curve for LY Preincubation of vascular smooth muscle cells with the phosphatidylinositol 3-kinase inhibitor LY (10, 50, and 100 μmol/L) demonstrated significant inhibition of thrombospondin-1 (TSP-1 )-, fibronectin (Fn )-, and vitronectin (Vn )-induced chemotaxis at 50 and 100 μmol/L. *P <.05 and **P <.005, compared with their respective uninhibited vascular smooth muscle cell chemotaxis toward TSP-1, Fn, or Vn. A representative experiment is shown. Journal of Vascular Surgery  , DOI: ( /mva ) Copyright © 2000 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

3 Fig. 2 Attenuation of vascular smooth muscle cell chemotaxis by phosphatidylinositol 3-kinase inhibition. Preincubation of vascular smooth muscle cells with the phosphatidylinositol 3-kinase inhibitor LY (100 μmol/L) significantly attenuated vascular smooth muscle cell chemotaxis toward thrombospondin-1 (TSP-1 ), fibronectin (Fn ), and vitronectin (Vn ), to a level not significantly different from vascular smooth muscle cells exposed to serum-free media (SFM ), P <.05. The chemoattractants TSP-1, Fn, and Vn (20 μg/mL) induced a significant increase in chemotaxis of uninhibited vascular smooth muscle cells, in comparison with SFM (P <.05). LY had no significant effect on the migration of vascular smooth muscle cells exposed to SFM. A representative experiment is shown. Experiments were performed in triplicate and repeated at least three times. *P <.05, compared with their respective uninhibited vascular smooth muscle cell chemotaxis toward TSP-1, Fn, or Vn. Journal of Vascular Surgery  , DOI: ( /mva ) Copyright © 2000 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

4 Fig. 3 Chemotaxis concentration curve for GF X. Preincubation of vascular smooth muscle cells with the protein kinase C inhibitor GF X (100 nmol/L, 1 μmol/L, and 5 μmol/L) demonstrated significant inhibition of thrombospondin-1 (TSP-1 )–induced chemotaxis at 1 and 5 μmol/L. *P <.05, compared with their respective uninhibited vascular smooth muscle cells chemotaxis toward TSP-1, Fn, or Vn. A representative experiment is shown. Journal of Vascular Surgery  , DOI: ( /mva ) Copyright © 2000 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

5 Fig. 4 Attenuation of vascular smooth muscle cell chemotaxis by protein kinase C inhibition. Preincubation of vascular smooth muscle cells with the protein kinase C inhibitor GF X (1 μmol/L) significantly attenuated vascular smooth muscle cell chemotaxis toward thrombospondin-1 (TSP-1 ; P <.05). The chemoattractants TSP-1, fibronectin (Fn ), and vitronectin (Vn ; 20 μg/mL) induced a significant increase in chemotaxis of uninhibited vascular smooth muscle cells in comparison with serum-free media (SFM ; P <.05). GF X had no significant effect on migration of vascular smooth muscle cells exposed to SFM. A representative experiment is shown. Experiments were performed in triplicate and repeated at least three times. *P <.05, compared with their respective uninhibited vascular smooth muscle cell chemotaxis toward TSP-1, Fn, or Vn. Journal of Vascular Surgery  , DOI: ( /mva ) Copyright © 2000 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

6 Fig. 5 A schematic representation of the potential involvement of phosphatidylinositol 3-kinase (PI3K ) and protein kinase C (PKC ) in thrombospondin-1 (TSP-1 )-, fibronectin (Fn )-, and vitronectin (Vn )-induced vascular smooth muscle cell (VSMC ) chemotaxis. PI3K may serve as an important signal transducer in chemotaxis triggered by the binding of TSP-1, Fn, or Vn. PI3K may relay its signaling via its interaction with G proteins, Ras, or mitogen-activated protein kinase (MAPK ). PKC is likely involved in signal transduction in TSP-1-induced VSMC chemotaxis, but not that of Fn or Vn. Journal of Vascular Surgery  , DOI: ( /mva ) Copyright © 2000 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

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